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Category: genetics

Scientists discover unknown organelle inside our cells

The discovery of an unknown organelle inside our cells could open the door to new treatments for devastating inherited diseases.

The , a type of specialized structure, has been dubbed a “hemifusome” by its discoverers at the University of Virginia School of Medicine and the National Institutes of Health. This little organelle has a big job helping our cells sort, recycle and discard important cargo within themselves, the scientists say. The new discovery could help scientists better understand what goes wrong in genetic conditions that disrupt these essential housekeeping functions.

“This is like discovering a new recycling center inside the cell,” said researcher Seham Ebrahim, Ph.D., of UVA’s Department of Molecular Physiology and Biological Physics. “We think the hemifusome helps manage how cells package and process material, and when this goes wrong, it may contribute to diseases that affect many systems in the body.”

Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast

Caffeine has long been associated with health benefits, including a reduced risk of age-related diseases. However, the specifics of how caffeine interacts with cellular mechanisms and nutrient and stress-responsive gene networks have remained elusive — until now.

In this pioneering research, published in the journal Microbial Cell, scientists used fission yeast, a single-celled organism with surprising similarities to human cells, to delve deeper into caffeine’s impact.

The researchers discovered that caffeine influences aging by engaging an ancient cellular energy system.

A few years ago, the same team found that caffeine prolongs cell life by acting on a growth regulator known as TOR (Target of Rapamycin). TOR is a molecular switch that regulates cell growth based on available food and energy and has been part of the evolutionary landscape for over 500 million years.

However, their latest study unveiled a surprising new finding: caffeine does not directly act on the TOR switch. Instead, it activates AMPK, a cellular fuel gauge that is conserved through evolution in both yeast and humans.

“When your cells are low on energy, AMPK kicks in to help them cope,” senior author Charalampos (Babis) Rallis, a reader in genetics, genomics and fundamental cell biology at Queen Mary University of London, said in a news release. “And our results show that caffeine helps flip that switch.”

Intriguingly, AMPK is also the target of metformin, a common diabetes medication currently under scrutiny for its potential to extend human lifespan when used alongside rapamycin.

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New AI Model Diagnoses Brain Tumors With 99% Accuracy, Without Surgery

An MRI scan revealed a brain tumor located in a difficult area, and performing a biopsy would carry significant risks for the patient, who had initially sought medical help due to double vision. Cases like this, discussed by a multidisciplinary team of cancer specialists, led researchers at Charité – Universitätsmedizin Berlin, along with their collaborators, to search for alternative diagnostic methods.

Their solution is an AI model that analyzes specific features in the genetic material of tumors, particularly their epigenetic fingerprint, which can be obtained from sources such as cerebrospinal fluid. As reported in the journal Nature Cancer, the model classifies tumors both rapidly and with high accuracy.

New study reveals genetic link between brain criticality and human cognition

A new study has revealed compelling evidence that brain criticality—a dynamic balance between neural excitation and inhibition—has a strong genetic foundation and is associated with cognitive performance. The research was published on June 23 in the Proceedings of the National Academy of Sciences.

Led by Prof. Liu Ning from the Institute of Biophysics of the Chinese Academy of Sciences (CAS) and Prof. Yu Shan from the Institute of Automation of CAS, the team analyzed resting-state functional MRI (rs-fMRI) data from the Human Connectome Project S1200 release. The dataset included 250 , 142 , and 437 unrelated individuals, providing a robust framework for examining the heritability of critical brain dynamics.

The results showed that brain criticality is significantly influenced by , with stronger genetic effects observed in primary sensory cortices compared to higher-order association regions. These findings suggest that the capacity of the brain to maintain near-critical dynamics—previously associated with optimal information processing and cognitive flexibility—is, to a substantial degree, inherited.

The Minds That Left Reality | Diaspora

Greg Egan’s Diaspora is one of the most ambitious and mind-bending science fiction novels ever published. It came out in 1997 and originally started as a short story called “Wang’s Carpets.” That story ended up as a chapter in the novel. Diaspora is: dense, smart, and way ahead of its time.
This is hard science fiction to the core. Egan invents entire new branches of physics. He reimagines life, consciousness, time, space — even what it means to be human. The book doesn’t ease you in. There’s a glossary, invented physics theories like Kozuch Theory, and characters that don’t even have genders. But if you stick with it, what you get isn’t just a story, it’s a look at what the future might actually become.
By the year 2,975, humanity isn’t one species anymore. It’s split into three groups: Fleshers: The biological humans, including the “statics” (unchanged baseline humans) and all sorts of heavily modified versions — underwater people, gene-hacked thinkers, even “dream apes” who gave up speech to live closer to nature. Gleisners: AIs in robotic bodies that live in space. They care about the physical world and experience time like regular humans. They’re kind of old-school — still sending ships to the stars, trying to build things in real space. Citizens: These are digital minds that live entirely in simulated worlds called polises.

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Diglycerides Are Associated With An Older Biological Age

And an increased all-cause mortality risk…

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Insulin on edge: Study identifies stress-triggered gene behind diabetes

Researchers from Osaka Metropolitan University have identified a gene that, when activated by metabolic stress, damages pancreatic β-cells—the cells responsible for insulin production and blood sugar control—pushing them toward dysfunction. The findings highlight a promising new target for early intervention in type 2 diabetes. The study is published in the Journal of Biological Chemistry.

While many factors can contribute to type 2 diabetes, lifestyle, especially diet, plays a major role in its onset. Genetics matter, but poor eating habits can greatly increase the risk of developing what is now often called a “silent epidemic.”

“Type 2 diabetes occurs when pancreatic β-cells, which secrete insulin to regulate , become impaired due to prolonged stress caused by poor dietary habits, a condition known as ,” said Naoki Harada, an associate professor at Osaka Metropolitan University’s Graduate School of Agriculture and lead author of this study.

Scientists use gene editing to correct harmful mitochondrial mutations in human cells

In a step toward treating mitochondrial diseases, researchers in the Netherlands have successfully edited harmful mutations in mitochondrial DNA using a genetic tool known as a base editor. The results, published in the open-access journal PLOS Biology, offer new hope for people with rare genetic conditions.

Mitochondria have their own small set of DNA. Mutations in this mitochondrial DNA can lead to a wide range of maternally inherited diseases, cancer, and aging-related conditions. While the development of CRISPR technology has given scientists new ways to correct mutations in nuclear DNA, this system cannot effectively cross the mitochondrial membrane and reach mitochondrial DNA.

In the new study, the researchers used a tool called a base editor—specifically, a DdCBE (double-stranded DNA deaminase toxin A-derived cytosine ). This tool allows scientists to change a single letter in the DNA code without cutting it, and it works on mitochondrial DNA.

Fusion superkine and focused ultrasound could enable targeted, noninvasive therapy for glioblastoma

Researchers at VCU Massey Comprehensive Cancer Center and the VCU Institute of Molecular Medicine (VIMM) have discovered a new and potentially revolutionary way to treat glioblastoma (GBM), the most aggressive type of brain cancer, which currently has no curative treatment options.

In a study led by Paul B. Fisher, MPh, Ph.D., FNAI, and Swadesh K. Das, Ph.D., recently published in the Journal for ImmunoTherapy of Cancer, researchers created a that demonstrates the ability to introduce a combination of treatment outcomes—direct toxicity and immunotoxicity—to kill the tumor while exploiting immunotherapy to potentially prevent the recurrence of GBM. The new molecule, a fusion superkine (FSK), contains dual-acting therapeutic cytokines in a single molecule.

“This is the tip of the iceberg,” said Dr. Fisher, the Thelma Newmeyer Corman Endowed Chair in Cancer Research at Massey, director of the VIMM and professor in the Department of Cellular, Molecular and Genetic Medicine. “We’re optimistic that our first trial in , planned for 2026, will show that the IL-24 gene and these therapeutic viruses are effective and safe. And [the FSK] will be the one knocking it out of the ballpark.